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Year : 2020  |  Volume : 14  |  Issue : 4  |  Page : 349-351

Yellow phosphorus poisoning and living donor liver transplant - A case report

Department of Liver Transplant Anesthesia, ASTER MIMS Hospital, Calicut, Kerala, India

Date of Submission11-Mar-2020
Date of Acceptance04-Oct-2020
Date of Web Publication30-Dec-2020

Correspondence Address:
Dr. Rakesh Babu
Consultant Liver transplant Anesthesia, Aster MIMS Hospital, Calicut - 673 016, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2470-7511.305423

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Acute liver failure due to yellow phosphorus is common in south India. Patients usually have an early asymptomatic phase and a rapidly progressing symptomatic phase. Early intensive care management can delay the progression to fulminant hepatic failure.Liver transplant is the only definitive management once fulminant hepatic failure sets in.

Keywords: Acute liver failure, liver transplant, ratol

How to cite this article:
Babu R, Kanianchalil K, Kumar A, Rajan R, Sahadevan S, Nambiar R. Yellow phosphorus poisoning and living donor liver transplant - A case report. Indian J Transplant 2020;14:349-51

How to cite this URL:
Babu R, Kanianchalil K, Kumar A, Rajan R, Sahadevan S, Nambiar R. Yellow phosphorus poisoning and living donor liver transplant - A case report. Indian J Transplant [serial online] 2020 [cited 2021 Apr 10];14:349-51. Available from: https://www.ijtonline.in/text.asp?2020/14/4/349/305423

  Introduction Top

Ratol paste is a common household rodenticide in South India. Its main component is yellow phosphorus. Cases of suicidal or accidental ingestion are common in a rural setup. Liver transplant is the only definite treatment once fulminant hepatic failure sets in.

We describe a case of suicidal ingestion of ratol paste which presented to our institute and its successful management with living donor liver transplant.

  Case Report Top

A 17-year-old girl was referred to our institute with a history of ingestion of ratol paste 3 days prior to admission. On admission, she was oriented to time, person, and place. There was a history of vomiting which was managed at a peripheral hospital. No history of abdominal pain, malena, or decreased urine output was noted. Blood pressure recorded was normal. The initial blood reports were also within the normal limits. She was admitted to the intensive care unit (ICU) for further care.

Intravenous fluids, antibiotics, antifungals, and antacids were started as per our institutional protocol. Anti-edema measures were started in the form of 3% sodium chloride infusion. Serial blood glucose monitoring was done to prevent hypoglycemia. N-acetyl cysteine infusion started according to the institutional protocol. Case was closely monitored for drop in urine put and features of encephalopathy. Laboratory testing of arterial ammonia, prothrombin time, international normalized ratio (INR) were done 8 th hourly and was closely monitored [Table 1].
Table 1: Laboratory values on day of surgery and immediate post operative period

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The patient developed features of encephalopathy along with worsening INR within 8 h of admission. She was intubated and electively ventilated and sedated. Management for acute liver failure (ALF) was continued. Arterial blood pressure monitoring and central lines were inserted in view of worsening clinical parameters. Since she met the King's College Criteria, plan for emergency transplant was decided. The mother was evaluated and found as a suitable donor and the team decided to proceed with living donor liver transplantation as life-saving option.

The MELD score on the day of surgery was 30. The surgery and intraoperative period was unremarkable. The total duration of surgery was 11 h. Graft/recipient weight ratio 0.9, warm ischemia 54 minutes. There were no significant intraoperative events. She was shifted to the transplant ICU for further management. Inotropic supports were continued to the postoperative period. The patient was extubated 14 h postsurgery once the blood lactate and arterial ammonia levels started a steady decline. Liver enzymes and INR started normalizing 3 days post transplant. There was no persistent acidosis during the immediate post transplant period. She was shifted out of ICU after 10 days and was discharged on 14th postoperative day.

  Discussion Top

Yellow phosphorus is a general protoplasmic toxin. Ratol paste contains approximately 2%–5% of yellow phosphorus. The estimated lethal dose to the liver is 1 mg/kg, and the ingestion of that amount results in death due to ALF and cardiovascular collapse. The clinical condition usually progresses in three stages: minor gastrointestinal symptoms for first 24 h, followed by asymptomatic 24–72 h and delayed presentation of fulminant liver failure after 72 h with high mortality.[1]

The toxins get absorbed through the intestinal tract and a majority of the total ingested dose concentrates into the liver where severe complications develop. Early gastric lavage is recommended to delay the absorption from the gastrointestinal tract. Toxin can reach the brain, striated muscle, and kidneys. Effects of intoxication include gastrointestinal symptoms, liver derangement, renal failure, arrhythmias, seizures, coma, and cardiovascular collapse.[2]

The only definitive treatment for ALF is liver transplantation because no antidote or medical treatment is available to reverse the toxic effects on the liver.

High mortality is due to the asymptomatic phase and patients presenting late to the emergency department with hepatic encephalopathy or severe gastrointestinal symptoms. The progress from asymptomatic phases to the symptomatic phase is usually rapid with worsening of liver enzymes and prothrombin time. Some cases develop a cute tubular necrosis and cardiac arrythmias, along with liver failure.

Our case had a late presentation to the hospital since she did not reveal the history of ratol ingestion. Since the early asymptomatic phase was easily missed, the initial supportive management was not done for her. Treatments with N acetyl-cysteine (NAC) infusion have shown to be effective supportive strategy.[3] NAC infusion could have slowed down the progression, as some case series have described the benefits of NAC infusion within 8 h of ingestion. N acetyl-cysteine acts by stimulating the glutathione synthesis and enhances glutathione transferase activity.

Once fulminant hepatic failure sets in liver transplant become the only life saver. Studies have shown that Meld score of over 31 on day 6 and onset encephalopathy at any time following ingestion are predictors for the need of liver transplant.[4]

Our case did not have any other organ system involvement and we decided for liver transplant once the Kings College Hospital criteria were met. Transplantation with multisystem involvement carries a high mortality. This case had a MELD 30 on days 5 and an INR of 7.11. There were no signs of toxic cardiomyopathy or acute renal failure.

Predictors of prognosis in these cases include the time of presentation, early treatment with NAC, amount of poison, early therapeutic plasma exchange, and absence of cardiac toxicity.

Early elevations in transaminase and alkaline phosphatase, a tenfold increase in alanine aminotransferase, and a severe derangement in prothrombin time all indicate poor prognosis.[5] Metabolic acidosis and hypoglycemia were significantly associated with mortality.[5]

Many centers use continuous renal replacement therapy (CRRT) as a bridge during the waiting period for a liver transplant. Our center did not have that option at that time period. An early CRRT could have prevented the worsening of encephalopathy.

Many transplant centers have a protocol for 5 cycles of therapeutic plasma exchange for ALF due to yellow phosphorous poison.[6] Such centers have done studies which has shown the benefit of plasma exchange in the setting of ALF.

Selection of cases for liver transplant is of utmost importance as cases can develop acute tubular necrosis and subsequent renal failure. Persistent hypotension due to toxic cardiomyopathy can be difficult to treat. Liver transplant in such cases can be futile. Availability of suitable donors within a short span of time is also a challenge as the timing of surgery is crucial.

Post transplant ICU stays can be prolonged, as the encephalopathy may take time to clear. These patients can have unusually prolonged ICU stays when compared to other cases of ALF due to the multiple systems involved by the toxins.

A successful outcome depends on early medical care, early initiation of liver-protective strategies like NAC infusion, and early recognition of features of encephalopathy and early referral to a transplant center.

Declaration of patient consent

The patient consent has been taken for participation in the study and for publication of clinical details and images. Patients understand that the names, initials would not be published, and all standard protocols will be followed to conceal their identity.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Brent J, Wallace KL, Burkhart KK. Phosphorus. In: Brent J, Wallace KL, Burkhart KK, Phillips SD, Donovan JW, editors. Critical Care Toxicology – Diagnosis and Management of the Critically Poisoned Patient. Philadelphia, PA: Elsevier Mosby; 2005. p. 851-61.  Back to cited text no. 1
Talley RC, Linhart JW, Trevino AJ, Moore L, Beller BM. Acute elemental phosphorus poisoning in man: Cardiovascular toxicity. Am Heart J 1972;84:139-40.  Back to cited text no. 2
Kafeel SI, Chandrasekaran VP, Eswaran V. Role of N-acetyl cystine in outcome of patients with YP poisoning: An observational study. Natl J Emerg Med 2012;1:35-40.  Back to cited text no. 3
Saraf V, Pande S, Gopalakrishnan U, Balakrishnan D, Menon RN, Sudheer OV, et al. Acute liver failure due to zinc phosphide containing rodenticide poisoning: Clinical features and prognostic indicators of need for liver transplantation. Indian J Gastroenterol 2015;34:325-9.  Back to cited text no. 4
Kharkongor MA, Mishra AK, Ninan KF, Iyadurai R. Early use of intravenous N-acetyl cysteine in treatment of acute yellow phosphorus poisoning. Curr Med Issues 2017;15:136-8.  Back to cited text no. 5
  [Full text]  
Banjan DS, Sane K, Wattamvar S, More M. Predictable factors for intervention with heparin free plasmapheresis in impending liver cell failure due to consumption of phosphorus rodenticide. Int J Res Med Sci 2019;7:3026-31.  Back to cited text no. 6


  [Table 1]


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